2048 The hypertrophic cardiomyopathy phenotype revisited with cardiovasculara magnetic resonance

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Meeting abstract

2048 The hypertrophic cardiomyopathy phenotype revisited with cardiovasculara magnetic resonance Martin S Maron*1, Evan Appelbaum2, Caitlin Harrigan3, Jacqueline Buros3, C Michael Gibson2, John R Lesser4, James E Udelson1, Warren J Manning2 and Barry J Maron4 Address: 1Tufts-New England Medical Center, Boston, MA, USA, 2Beth Isreal Deaconess Medical Center and Perfuse Core Laboratory and Data Processing Center, Boston, MA, USA, 3Perfuse Core Laboratory and Data Processing Center, Boston, MA, USA and 4Minneapolis Heart Institute Foundation, Minneapolis, MN, USA * Corresponding author

from 11th Annual SCMR Scientific Sessions Los Angeles, CA, USA. 1–3 February 2008 Published: 22 October 2008 Journal of Cardiovascular Magnetic Resonance 2008, 10(Suppl 1):A317

doi:10.1186/1532-429X-10-S1-A317

Abstracts of the 11th Annual SCMR Scientific Sessions - 2008

Meeting abstracts – A single PDF containing all abstracts in this Supplement is available here. http://www.biomedcentral.com/content/pdf/1532-429X-10-S1-info.pdf

This abstract is available from: http://jcmr-online.com/content/10/S1/A317 © 2008 Maron et al; licensee BioMed Central Ltd.

Introduction Hypertrophic cardiomyopathy (HCM) is generally regarded as a disease characterized by substantial left ventricular (LV) wall thickening, often with extensive hypertrophy diffusely involving the LV chamber. This impression has been based on traditional non-tomographic imaging with two-dimensional echocardiography. However, CMR has certain advantages for more precisely defining LV hypertrophy and the phenotypic expression of HCM.

Purpose To define the distribution and pattern of LV wall thickening in HCM using CMR.

Methods CMR was performed in 82 consecutive HCM patients (42 ± 16 years; 71% male) from two HCM referral centers. ECG-gated, breath-hold cine images were acquired in 3 long-axes and contiguous 10 mm thick short-axis slices, achieving full LV coverage. LV was divided into 16 segments based on the established AHA model. For each short-axis cross-sectional level of the LV (basal, mid, apical) the greatest wall thickness measurement was calculated in each wall segment. LV hypertrophy was defined as wall thickness ≥ 15 mm and: focal when confined to ≤ 2 contiguous segments (≤ 12% of LV), intermediate if

present in 3–7 segments (13–49% of LV) and diffuse when present in ≥ 8 segments (≥ 50% of LV).

Results Maximal LV wall thickness was 22 ± 4.5 mm (range 15 to 36 mm). Basal anterior septum and contiguous anterior free wall were the most common areas. Distribution and extent of hypertrophied LV segments was focal in 16 (19%), intermediate in 30 (35%) and diffuse in 39 (46%). Sixteen patients (19%) also had areas of non-contiguous LV hypertrophy separated by regions of normal thickness. A significant relationship was evident between the number of hypertrophied LV segments and total LV mass (r2 = 0.6; p < 0.001). However, no correlation was evident between distribution of LV hypertrophy and a variety of demographic